Discover. Oncology最新文献

{"title":"Targeting the insulin-like growth factor-1 receptor to overcome imatinib resistance in chronic myeloid leukemia.","authors":"Seiichi Okabe, Yuya Arai, Akihiko Gotoh","doi":"10.1007/s12672-024-01706-6","DOIUrl":"https://doi.org/10.1007/s12672-024-01706-6","url":null,"abstract":"<p><p>Patients with chronic myeloid leukemia (CML) frequently develop resistance to tyrosine kinase inhibitors such as imatinib. In this study, we explored the role of the insulin-like growth factor 1 (IGF-1) signaling pathway in CML and imatinib resistance. An analysis of IGF-1 gene expression using public databases revealed elevated levels of insulin-like growth factor-binding proteins in patients with chronic-phase CML. Further research revealed that IGF-1-related genes were upregulated in patients who were unresponsive to imatinib, suggesting that IGF-1 signaling plays a role in the resistance mechanism. Furthermore, we evaluated the efficacy of linsitinib, a selective insulin-like growth factor-1 receptor (IGF-1R) inhibitor, in inhibiting the growth of CML cell lines, including imatinib-resistant cell lines, and observed a notable decrease in cell viability and an increase in cytotoxicity. The combination of imatinib and linsitinib reduced cell viability and increased caspase-3/7 activity in imatinib-resistant cells. Moreover, silencing of IGF-1R by small interfering ribonucleic acid increased the sensitivity of CML cell lines to imatinib, indicating that IGF-1R could be a strategic target for overcoming resistance. These findings highlight the therapeutic potential of linsitinib and that IGF-1R inhibition may improve the treatment outcomes of patients with imatinib-resistant CML.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"15 1","pages":"835"},"PeriodicalIF":2.8,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142885254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nuclear receptor profiling for subtype classification and as prognostic markers in 33 cancer types.","authors":"Kazuya Nakamichi, Hironori Suzuki, Yusuke Yamamoto, Kentaro Semba, Jun Nakayama","doi":"10.1007/s12672-024-01732-4","DOIUrl":"https://doi.org/10.1007/s12672-024-01732-4","url":null,"abstract":"<p><p>Nuclear receptors, a group of 48 transcription factors that regulate a multitude of processes within our body, have long been employed as diagnostic markers or therapeutic targets in breast cancer, prostate cancer, and acute promyelocytic leukemia. Unfortunately, no comprehensive investigation has been conducted on their significance in other cancer types. The current study aimed to explore novel diagnostic markers by classifying nuclear receptors according to their expression patterns based on transcriptome data from The Cancer Genome Atlas on 10,071 tumor samples across 33 cancer types and investigating their association with genetic mutations, histological types, and prognosis. Our analysis showed that 21 cancers, including breast cancer, can be classified into distinct clusters based on their nuclear receptor expression profiles. Moreover, significant differences in overall survival were observed in 9 of the 21 cancer types. Overall, the results of this study indicate that previously overlooked nuclear receptors, such as NR0B1 in lung adenocarcinoma, may prove beneficial in the diagnosis of several cancers.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"15 1","pages":"834"},"PeriodicalIF":2.8,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142881473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RASGEF1C as a novel prognostic biomarker for LUAD.","authors":"Jinlong Liu, Xiaoying Liu, Yingou Zeng, Di Qiao, Bin Dai, Yunlong Wu, Meng Wang, Qiang Wang","doi":"10.1007/s12672-024-01718-2","DOIUrl":"https://doi.org/10.1007/s12672-024-01718-2","url":null,"abstract":"<p><p>Lung adenocarcinoma (LUAD) is a common histologic lung cancer with high morbidity and mortality, and most patients have distant metastases at diagnosis. RasGEF Domain Family Member 1C (RASGEF1C) could regulated Alzheimer's disease. However, its function in various cancers, including LUAD, is poorly understood. In the present study, we discovered that high expression of RASGEF1C in LUAD was associated with poorer prognosis, unfavorable histological features, and poorer pathological staging. In addition, RASGEF1C expression was an independent predictor of overall survival, disease specific survival, and progress free interval in patients with LUAD. High expression of RASGEF1C was linked to signaling pathways that are involved in the immune response and cell proliferation, according to KEGG enrichment analysis. Additionally, we verified that RASGEF1C was highly expressed in LUAD cell lines and that RASGEF1C knockdown dramatically decreased the capacity of LUAD cell lines to invade, migrate, and proliferate. Our research provides mechanistic insights into the function of RASGEF1C in the progression of LUAD and suggests that RASGEF1C is a prospective target for future therapy.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"15 1","pages":"825"},"PeriodicalIF":2.8,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical and imaging characteristics of intraductal papillary neoplasms of the breast: a prospective trial.","authors":"Yingjiao Wang, Yuechong Li, Yang Qu, Yidong Zhou, Qiang Sun, Songjie Shen","doi":"10.1007/s12672-024-01681-y","DOIUrl":"https://doi.org/10.1007/s12672-024-01681-y","url":null,"abstract":"<p><strong>Background: </strong>Intraductal papillary neoplasms (IPNs) often have a similar clinical and imaging presentation, making them difficult to diagnose. We designed this study to refine and compare intraductal papillary neoplasms' clinical and imaging characteristics.</p><p><strong>Methods: </strong>This study included a total of 154 patients with a postoperative diagnosis of IPNs and collected their clinical, imaging, and pathological data. We compared the clinical and imaging characteristics of benign, atypical hyperplasia, and malignant lesions. We also compared the diagnostic efficacy of ultrasound and mammography.</p><p><strong>Results: </strong>The mean age of malignant patients was 57 years old, which was significantly higher than that in the other groups (48 years in the benign group and 47 years in the atypical hyperplasia group). The proportion of patients with malignant lesions clinically presenting as palpable masses (31.3%) was significantly higher than that of benign lesions (8.6%) (P < 0.05). The proportion of malignant lesions presenting in the periphery (≥ 3 cm from the nipple) was 40.6% compared to 22.4% for benign (P < 0.05). In ultrasonography, characteristics that showed statistically significant differences between benign and malignant lesions were the shape of the mass and calcification (P < 0.05). On mammography, differences were found in mass shape, calcification, and density of masses and glands (P < 0.05).</p><p><strong>Conclusions: </strong>Clinical features such as age, symptoms, lesion location, and imaging characteristics such as shape, calcification, mass, and density may help to differentiate the classifications of IPNs.</p><p><strong>Trial registration: </strong>This study was registered at ClinicalTrials.gov on 12/06/2020 (identifier: NCT04429269).</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"15 1","pages":"831"},"PeriodicalIF":2.8,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142881451","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated analysis of cell cycle and p53 signaling pathways related genes in breast, colorectal, lung, and pancreatic cancers: implications for prognosis and drug sensitivity for therapeutic potential.","authors":"Jiyauddin Khan, Priyanjana Ghosh, Urmi Bajpai, Kountay Dwivedi, Daman Saluja","doi":"10.1007/s12672-024-01712-8","DOIUrl":"https://doi.org/10.1007/s12672-024-01712-8","url":null,"abstract":"<p><p>Cancer, a leading cause of death worldwide, is projected to increase by 76.6% in new cases and 89.7% in mortality by 2050 (WHO 2022). Among various types, lung cancer is the most prevalent with high morbidity, while breast, colorectal, and pancreatic cancers also show high mortality rates. Cancer progression often involves disruption in cell cycle regulation and signaling pathways, with mutations in genes like TP53, EGFR, and K-RAS playing significant roles. In this study, we analyzed gene expression datasets to identify common molecular signatures across breast, colorectal, lung and pancreatic cancers. Our focus was on genes related to cell cycle regulation and p53 signaling pathway, intending to discover potential biomarkers for improved diagnosis and treatment strategies. The study analyzed GEO datasets; GSE45827, GSE9348, GSE30219, and GSE62165 for breast, colorectal, lung, and pancreatic cancers respectively. Differentially expressed genes (DEGs) were identified using GEO2R, and functional annotation and pathway analysis were performed using WebGestalt. Common cell cycle and p53 signaling genes were acquired from MSigDB using GSEA. A protein-protein interaction network was constructed using STRING and Cytoscape, identifying top hub genes. Validation of hub genes at mRNA and protein levels was done via GEPIA2 and Human Protein Atlas. Survival analysis was conducted using TCGA data by GEPIA2 and LASSO, and drug sensitivity was analyzed with the GSCA drug bank database, highlighting potential therapeutic targets. The study identified 411 common DEGs among these four cancers. Pathway and functional enrichment revealed key biological processes and pathways like p53 signaling, and cell cycle. The intersection of these DEGs with genes involved in cell cycle and p53 signaling, identified 23 common genes that were used for constructing a PPI network. The top 10 hub genes were validated both for mRNA and protein expression, revealing they are significantly overexpressed in all studied cancers. Prognostic relevance showed that MCM4, MCM6, CCNA2, CDC20, and CHEK1 are associated with survival. Additionally, drug sensitivity analysis highlighted key gene-drug interactions, suggesting potential targets for therapeutic intervention.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"15 1","pages":"832"},"PeriodicalIF":2.8,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142881466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploration of the shared pathways and common biomarkers in cervical and ovarian cancer using integrated bioinformatics analysis.","authors":"Fang Liu, Min Wang, Tian Zhu, Cong Xu, Guangming Wang","doi":"10.1007/s12672-024-01725-3","DOIUrl":"https://doi.org/10.1007/s12672-024-01725-3","url":null,"abstract":"<p><strong>Objective: </strong>Searching for potential biomarkers and therapeutic targets for early diagnosis of gynecological tumors to improve patient survival.</p><p><strong>Methods: </strong>Microarray datasets of cervical cancer (CC) and ovarian cancer (OC) were downloaded from the Gene Expression Omnibus (GEO) database, then, differential gene expression between cancerous and normal tissues in the datasets was analyzed. Weighted gene co-expression network analysis (WGCNA) was performed to screen for co-expression modules associated with CC and OC. The screened shared genes were then further analyzed for functional pathway enrichment. Next, the least absolute shrinkage and selection operator (LASSO) with tenfold cross validation is used to further screened for common diagnostic biomarkers for the two diseases, and further validation is performed using two independent GEO datasets. Finally, the CIBERSORT algorithm was used to estimate the immune infiltration levels of CC and OC, and the correlation between immune cell infiltration and common biomarkers was explored.</p><p><strong>Results: </strong>After crossing the common DEGs detected by \"Limma\" R package with the common module genes identified by WGCNA, 44 shared genes were obtained. Functional enrichment indicates that these shared genes are mainly related to DNA synthesis pathways. Lasso regression analysis revealed that EFNA1, TYMS, and WISP2 were co-diagnostic markers for CC and OC, and then based on their expression levels and diagnostic efficacy, EFNA1 was selected as the best co-marker for CC and OC. Immune infiltration analysis shows that the immune environment has a significant impact on the occurrence and development of CC and OC, and the expression of EFNA1 is related to changes in immune cells. Gene-drug interaction analyses identified 27 common drug compounds that interact with candidate genes.</p><p><strong>Conclusion: </strong>This study adopted bioinformatics methods to investigate the common pathways and identify diagnostic markers between CC and OC, suggesting that DNA synthesis and immune environment are closely related to the occurrence and development of CC and OC. EFNA1 may be a potential diagnostic indicator and therapeutic target for patients with CC and OC.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"15 1","pages":"826"},"PeriodicalIF":2.8,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Machine learning-based identification of histone deacetylase-associated prognostic factors and prognostic modeling for low-grade glioma.","authors":"Keshan Wen, Weijie Zhu, Ziyi Luo, Wei Wang","doi":"10.1007/s12672-024-01713-7","DOIUrl":"https://doi.org/10.1007/s12672-024-01713-7","url":null,"abstract":"<p><strong>Background: </strong>Low-grade glioma (LGG) is a slow-growing but invasive tumor that affects brain function. Histone deacetylases (HDACs) play a critical role in gene regulation and tumor progression. This study aims to develop a prognostic model based on HDAC-related genes to aid in risk stratification and predict therapeutic responses.</p><p><strong>Methods: </strong>Expression data from The Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas (CGGA) were analyzed to identify an optimal HDAC-related risk signature from 73 genes using 10 machine learning algorithms. Patients were stratified into high- and low-risk groups based on the median risk score. Prognostic accuracy was evaluated using Kaplan-Meier survival analysis and receiver operating characteristic (ROC) curves. Functional enrichment analyses, including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and Gene Set Enrichment Analysis (GSEA), were performed to explore pathways linked to the gene signature. Immune infiltration and tumor microenvironment characteristics were assessed using Single Sample Gene Set Enrichment Analysis (ssGSEA) and ESTIMATE algorithm. SubMap was applied to predict responsiveness to immune checkpoint inhibitors, and chemotherapeutic sensitivity was analyzed via the Genomics of Drug Sensitivity in Cancer (GDSC) database.</p><p><strong>Results: </strong>A prognostic model consisting of four HDAC-related genes-SP140, BAZ1B, SP100, and SIRT1-was identified. This signature displayed strong prognostic accuracy, achieving a C-index of 0.945. Individuals with LGG were systematically divided into high-risk and low-risk cohorts based on the median risk value, enabling more precise risk stratification. The survival prognosis was significantly worse in the high-risk cohort compared to the low-risk group, highlighting distinct survival trajectories. Notably, the two cohorts exhibited marked shifts in immune checkpoint gene transcriptional profiles and immune cell infiltration maps, underscoring fundamental biological differences that contribute to these differing prognoses.</p><p><strong>Conclusion: </strong>We developed an HDAC-related four-gene prognostic model that correlates with survival, immune landscape, and therapeutic response in LGG patients. This model may guide personalized treatment strategies and improve prognostic accuracy, warranting further validation in clinical settings.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"15 1","pages":"824"},"PeriodicalIF":2.8,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Programmed cell death pathways in lung adenocarcinoma: illuminating tumor drug resistance and therapeutic opportunities through single-cell analysis.","authors":"Long Li, Shancheng He","doi":"10.1007/s12672-024-01736-0","DOIUrl":"https://doi.org/10.1007/s12672-024-01736-0","url":null,"abstract":"<p><p>Lung adenocarcinoma (LUAD) is a major contributor to cancer-related deaths, distinguished by its pronounced tumor heterogeneity and persistent challenges in overcoming drug resistance. In this study, we utilized single-cell RNA sequencing (scRNA-seq) to dissect the roles of programmed cell death (PCD) pathways, including apoptosis, necroptosis, pyroptosis, and ferroptosis, in shaping LUAD heterogeneity, immune infiltration, and prognosis. Among these, ferroptosis and pyroptosis were most significantly associated with favorable survival outcomes, highlighting their potential roles in enhancing anti-tumor immunity. Distinct PCD-related LUAD subtypes were identified, characterized by differential pathway activation and immune cell composition. Subtypes enriched with cytotoxic lymphocytes and dendritic cells demonstrated improved survival outcomes and increased potential responsiveness to immunotherapy. Drug sensitivity analysis revealed that these subtypes exhibited heightened sensitivity to targeted therapies and immune checkpoint inhibitors, suggesting opportunities for personalized treatment strategies. Our findings emphasize the interplay between PCD pathways and the tumor microenvironment, providing insights into the mechanisms underlying tumor drug resistance and immune evasion. By linking molecular and immune features to clinical outcomes, this study highlights the potential of targeting PCD pathways to enhance therapeutic efficacy and overcome resistance in LUAD. These results contribute to a growing framework for developing precise and adaptable cancer therapies tailored to specific tumor characteristics.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"15 1","pages":"828"},"PeriodicalIF":2.8,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876430","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the role of Disulfidptosis in glioma progression: insights into tumor heterogeneity and therapeutic potential through single-cell RNA sequencing.","authors":"Xiaorong Fan, Maojun Chen","doi":"10.1007/s12672-024-01685-8","DOIUrl":"https://doi.org/10.1007/s12672-024-01685-8","url":null,"abstract":"<p><strong>Background: </strong>Gliomas, particularly glioblastoma (GBM), are the most common and aggressive primary brain tumors in adults, characterized by high malignancy and frequent recurrence. Despite standard treatments, including surgery, radiotherapy, and chemotherapy, the prognosis for GBM remains poor, with a median survival of less than 15 months and a five-year survival rate below 10%. Tumor heterogeneity and resistance to treatment create significant challenges in controlling glioma progression. Therefore, there is an urgent need for new therapeutic targets and strategies.</p><p><strong>Objective: </strong>This study investigates the role of Disulfidptosis, a recently discovered form of programmed cell death, in gliomas. Unlike apoptosis and necrosis, Disulfidptosis is driven by the abnormal accumulation of intracellular disulfide bonds, leading to protein misfolding and cytoskeletal collapse, particularly in cancer cells with metabolic dysregulation. We aim to explore how glioma cells respond to Disulfidptosis and identify potential therapeutic targets by analyzing the heterogeneity of gliomas at the single-cell level using single-cell RNA sequencing (scRNA-seq).</p><p><strong>Methods: </strong>scRNA-seq data from glioma patients were analyzed to uncover differences in ferroptosis-related pathways, including iron metabolism and lipid peroxidation. Cellular subpopulations within gliomas were profiled to assess their sensitivity to Disulfidptosis and the underlying mechanisms. Survival analysis was conducted to evaluate the clinical relevance of Disulfidptosis-related gene expression.</p><p><strong>Results: </strong>Multiple cell subpopulations within gliomas exhibit varying sensitivities to Disulfidptosis, influenced by their metabolic properties. Dysregulated iron metabolism and antioxidant mechanisms were identified as key factors impacting Disulfidptosis sensitivity. Glioma microenvironment signaling pathways also play a role in regulating Disulfidptosis. These findings suggest that activating Disulfidptosis pathways may provide novel therapeutic strategies to overcome treatment resistance in gliomas.</p><p><strong>Conclusion: </strong>This study offers new insights into the role of Disulfidptosis in glioma progression and highlights its potential as a therapeutic target. By leveraging single-cell sequencing data, the research uncovers tumor heterogeneity and identifies specific cell populations resistant to Disulfidptosis. These findings may pave the way for personalized treatment strategies to improve survival outcomes in glioma patients.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"15 1","pages":"829"},"PeriodicalIF":2.8,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Systematic pan-cancer analysis identifies ZBTB11 as a potential pan-cancer biomarker and immunotherapy target in multiple tumor types.","authors":"Peiyi Xu, Qiuyan Zhang, Jing Zhai, Pu Chen, Xueting Deng, Lin Miao, Xiuhua Zhang","doi":"10.1007/s12672-024-01697-4","DOIUrl":"https://doi.org/10.1007/s12672-024-01697-4","url":null,"abstract":"<p><strong>Background: </strong>ZBTB11 is a putative transcription factor with an N-terminal BTB domain and tandem C-terminal zinc finger motifs. Recent studies have suggested a potential role for ZBTB11 in tumorigenesis. However, the biological significance of ZBTB11 in different cancer types remains uncertain.</p><p><strong>Methods: </strong>The expression levels, prognostic values, genetic mutations, and DNA promoter methylation of ZBTB11 across tumor types were explored via various online websites and databases, including TIMER2.0, GEPIA2, cBioPortal, UALCAN, GSCA, CancerSEA, and others. Additionally, a competing lncRNA-miRNA network of ZBTB11 was constructed, and its interaction with chemicals and genes was investigated.</p><p><strong>Results: </strong>Our findings revealed that ZBTB11 was aberrantly expressed in a multitude of tumor types and exhibited variability across various tumor stages. A survival analysis revealed that ZBTB11 predicted a poor prognosis in BRCA, KIRP, LIHC, PCPG, PRAD, SARC, UCEC, and a good prognosis in CHOL, ESCA, GBM, KIRC, and READ. We also found that the most frequent genetic alterations type of ZBTB11 was mutation, and the DNA methylation level of ZBTB11 decreased in various cancers. Furthermore, ZBTB11 expression correlated with immune cells infiltration and genetic markers of immunodulators in cancers. Moreover, the results of single-cell sequencing demonstrated that ZBTB11 could regulate several tumor biological behaviors, including apoptosis, DNA damage, and angiogenesis. A lncRNA-miRNA network regulating ZBTB11 expression in tumor development and progression was constructed. It is of particular significance that ZBTB11 demonstrated a correlation with the CTRP and GDSC drug sensitivity, and that it served as a mediator between chemicals and cancers.</p><p><strong>Conclusion: </strong>These findings demonstrate that ZBTB11 is associated with multiple tumor types and disease prognosis. ZBTB11 may represent a potential key biomarker and therapeutic target in cancers.</p>","PeriodicalId":11148,"journal":{"name":"Discover. Oncology","volume":"15 1","pages":"830"},"PeriodicalIF":2.8,"publicationDate":"2024-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142881488","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}